首页> 外文期刊>International Journal of Radiation Biology: Covering the Physical, Chemical, Biological, and Medical Effects of Ionizing and Non-ionizing Radiations >Melatonin reduces X-ray radiation-induced lung injury in mice by modulating oxidative stress and cytokine expression
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Melatonin reduces X-ray radiation-induced lung injury in mice by modulating oxidative stress and cytokine expression

机译:褪黑激素通过调节氧化应激和细胞因子表达来减少小鼠X射线辐射诱导的肺损伤

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Purpose: The modification of radiation-induced lung injuries by melatonin was studied by measuring changes in oxidative stress, cytokine expression and histopathology in the lung tissue of mice following irradiation. Materials and methods: The thoraces of C57BL/6 mice were exposed to a single X-ray radiation dose of 12 Gy with or without 200 mg/kg of melatonin pretreatment. The level and localization of transforming growth factor (TGF)-??1 protein were measured using an enzyme-linked immunosorbent assay (ELISA) method and immunohistochemical staining, respectively. Real-time quantitative polymerase chain reaction (PCR) was established to evaluate the relative mRNA expression levels of TGF-??1, tumor necrosis factor (TNF)-??, interleukin (IL)-1?? and IL-6. Results: Malondialdehyde (MDA) levels increased after irradiation and then significantly reduced (1.9-fold) under melatonin treatment. Changes in superoxide dismutase (SOD) and catalase activities, as well as glutathione (GSH) levels, after irradiation were significantly reduced by melatonin, including a notable 5.4-fold difference in catalase activity. We observed increased expression of TGF-??1 and TNF-?? after irradiation and a significant reduction in the elevation of their expression by melatonin treatment. Furthermore, irradiation-induced histopathologic alterations were obviously abated in the melatonin-pretreated mice. Conclusions: The present results suggest that melatonin reduces radiation-induced lung injury via a significant reduction of oxidative stress and of the production of cytokines, such as TGF-??1 and TNF-??, the production of which increased following lung irradiation. ? 2013 Informa UK, Ltd.
机译:目的:通过测量照射后小鼠肺组织中的氧化应激,细胞因子表达和组织病理学的变化来研究褪黑激素的辐射诱导的肺损伤。材料和方法:将C57BL / 6小鼠的父母暴露于12Gy的单个X射线辐射剂量,或者没有200mg / kg褪黑激素预处理。使用酶联免疫吸附测定(ELISA)方法和免疫组织化学染色来测量转化生长因子(TGF) - β1蛋白的水平和定位。建立实时定量聚合酶链反应(PCR),以评估TGF的相对mRNA表达水平 - -?? 1,肿瘤坏死因子(TNF) - - ??,白细胞介素(IL)-1 ??和IL-6。结果:麦冬醛(MDA)水平在辐照后增加,然后在褪黑激素处理下显着降低(1.9倍)。通过褪黑素显着减少过滤歧化酶(SOD)和过氧化氢酶活性(SOD)和过氧化氢酶活性,以及​​谷胱甘肽(GSH)水平的变化,包括褪黑素显着降低过氧化氢酶活性的值为5.4倍。我们观察到TGF的表达增加 - ?? 1和TNF- ??褪黑素治疗辐照和其表达升高的显着减少。此外,在褪黑激素 - 预处理的小鼠中显然消除了辐照诱导的组织病理学改变。结论:目前的结果表明,褪黑素通过显着降低氧化应激和细胞因子的产生减少辐射诱导的肺损伤,例如TGF - - ?? 1和TNF - ??,其产生在肺照射后增加。还2013年Informa UK,Ltd。

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